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Journal articles on the topic 'Fusions ETS'

Author: Grafiati

Published: 7 July 2024

Last updated: 31 July 2025

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1

Smith, Jenny L., Rhonda E. Ries, Yi-Cheng Wang, et al. "ETS Family Transcription Factor Fusions in Childhood AML: Distinct Expression Networks and Clinical Implications." Blood 138, Supplement 1 (2021): 2356. http://dx.doi.org/10.1182/blood-2021-148894.

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Abstract The ETS family of genes encode transcription factors (TFs) containing the ETS DNA binding domain, which have roles in cellular growth and development, including embryonic hematopoiesis. Dysregulation of these genes is associated with malignant transformation and tumorigenesis. In childhood acute myeloid leukemia (AML), the MNX1-ETV6 t(7;12)(q36;p13) and FUS-ERG t(16;21)(p11;q22) fusions are associated with adverse outcome. However, the biological and clinical implications of other ETS oncofusions in pediatric AML remain unknown. We identified 62 ETS gene fusions in 1,473 primary diagn

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2

Barbi de Moura, Michelle, Fadel S. Alyaqoub, Gargi D. Basu, et al. "Erythroblast transformation-specific transcription factor fusions in prostate cancer." Journal of Clinical Oncology 41, no. 6_suppl (2023): 224. http://dx.doi.org/10.1200/jco.2023.41.6_suppl.224.

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224 Background: Common drivers in advanced prostate cancer (PC) involve fusions of the 3’ DNA binding domain-containing region of an Erythroblast Transformation Specific (ETS) transcription factor gene with a 5’ region of another gene, often one that is androgen-regulated. Previous work indicates that PCs harboring TMPRSS2:ERG fusions are more dependent on androgen signaling, and men with such tumors may, therefore, be more responsive to the effects of androgen deprivation therapy than men lacking this fusion. In this study, we examined the frequency of fusions involving ETS-family genes, incl

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3

Staege, Martin S., and Daniela Max. "Genetics and Epigenetics of the TET-ETS Translocation Network." Genetics & Epigenetics 2 (January 2009): GEG.S2815. http://dx.doi.org/10.4137/geg.s2815.

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In the present paper we review the translocation network involving TET and ETS family members with special focus on the Ewing family of tumors. FUS (fusion, involved in t(12;16) in malignant liposarcoma = TLS, Translocated in liposarcoma), EWSR1 (Ewing sarcoma breakpoint region 1) and TAF15 (TATA box-binding protein-associated factor, 68-KD) are the three human members of the TET family of RNA binding proteins. In addition, two EWSR1 pseudogenes are present in the human genome. TET family members are involved in several oncogenic gene fusions. Five of the 18 known fusion partners belong to the

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4

Wei, Ting, Ji Lu, Tao Ma, Haojie Huang, Jean-Pierre Kocher, and Liguo Wang. "Re-Evaluate Fusion Genes in Prostate Cancer." Cancer Informatics 20 (January 2021): 117693512110275. http://dx.doi.org/10.1177/11769351211027592.

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Background: Thousands of gene fusions have been reported in prostate cancer, but their authenticity, incidence, and tumor specificity have not been thoroughly evaluated, nor have their genomic characteristics been carefully explored. Methods: We developed FusionVet to dedicatedly validate known fusion genes using RNA-seq alignments. Using FusionVet, we re-assessed 2727 gene fusions reported from 36 studies using the RNA-seq data generated by The Cancer Genome Atlas (TCGA). We also explored their genomic characteristics and interrogated the transcriptomic and DNA methylomic consequences of the

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5

De Cecco, Federica, Lidia Chellini, Veronica Riccioni, and Maria Paola Paronetto. "Oncogenic Fusions Harboring ETS Genes: Exploring Novel Targetable Opportunities in Prostate Cancer." Cancers 17, no. 10 (2025): 1657. https://doi.org/10.3390/cancers17101657.

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Chromosomal rearrangements are implicated in the pathogenesis of several human malignancies, but, concurrently, they also represent targetable opportunities, as exemplified by imatinib (Gleevec), which targets the BCR-ABL gene fusion in myeloid leukemia. In prostate cancer, several chromosomal rearrangements have been identified, most of them involving ETS genes, which encode key transcription factors. In this review, we explore the discovery of 5′ partners that classify ETS gene fusions into distinct groups based on the prostate specificity and androgen responsiveness. Furthermore, we try to

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6

Gasi Tandefelt, Delila, Joost Boormans, Karin Hermans, and Jan Trapman. "ETS fusion genes in prostate cancer." Endocrine-Related Cancer 21, no. 3 (2014): R143—R152. http://dx.doi.org/10.1530/erc-13-0390.

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Prostate cancer is very common in elderly men in developed countries. Unravelling the molecular and biological processes that contribute to tumor development and progressive growth, including its heterogeneity, is a challenging task. The fusion of the genes ERG and TMPRSS2 is the most frequent genomic alteration in prostate cancer. ERG is an oncogene that encodes a member of the family of ETS transcription factors. At lower frequency, other members of this gene family are also rearranged and overexpressed in prostate cancer. TMPRSS2 is an androgen-regulated gene that is preferentially expresse

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7

Anderson, Nathaniel D., Richard de Borja, Matthew D. Young, et al. "Rearrangement bursts generate canonical gene fusions in bone and soft tissue tumors." Science 361, no. 6405 (2018): eaam8419. http://dx.doi.org/10.1126/science.aam8419.

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Sarcomas are cancers of the bone and soft tissue often defined by gene fusions. Ewing sarcoma involves fusions between EWSR1, a gene encoding an RNA binding protein, and E26 transformation-specific (ETS) transcription factors. We explored how and when EWSR1-ETS fusions arise by studying the whole genomes of Ewing sarcomas. In 52 of 124 (42%) of tumors, the fusion gene arises by a sudden burst of complex, loop-like rearrangements, a process called chromoplexy, rather than by simple reciprocal translocations. These loops always contained the disease-defining fusion at the center, but they disrup

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8

Buteyn, Nathaniel J., Connor Burke, Eve Gardner, et al. "Reclassification of ETS Family Transcription Factor Fusions in Pediatric AML Based on Molecular Drivers." Blood 142, Supplement 1 (2023): 4298. http://dx.doi.org/10.1182/blood-2023-189474.

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Pediatric Acute Myeloid Leukemia (pAML) patients with a fusion involving an E26 transformation-specific (ETS) transcription factor have traditionally been considered high-risk. The most common fusions include ETV6::MNX1 t(7;12)(q36;p13) and FUS::ERG t(16;21)(p11;q22), yet primary fusion alone has proven incapable of predicting response to treatment. Indeed, within the 60 pAML patients with ETS fusions from the Children's Oncology Group (COG) trials AAML0531 and AAML1031, there were 25 unique fusions and diverse outcomes between patients who did share a primary fusion. A molecular based reclass

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9

Lawlor, E. R., J. A. Mathers, T. Bainbridge, et al. "Peripheral primitive neuroectodermal tumors in adults: documentation by molecular analysis." Journal of Clinical Oncology 16, no. 3 (1998): 1150–57. http://dx.doi.org/10.1200/jco.1998.16.3.1150.

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PURPOSE The Ewing tumor (ET) family of peripheral primitive neuroectodermal tumors (pPNETs) are primitive small round-cell tumors (SRCTs) of the bone and soft tissue that occur predominantly in children and adolescents. However, pPNETs only rarely enter the differential diagnosis of bone and soft tissue SRCTs in adults. Recently, gene fusions between the EWS gene and different members of the ETS transcription factor family have been shown to occur in virtually all pPNETs and thus constitute a pathognomonic marker for this tumor subclass. The aim of the present study was to document EWS/ETS fus

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10

Downing, Nicholas F., Kaitlyn M. Mills, and Peter C. Hollenhorst. "Abstract 3033: Oncogenic ETS transcription factors avoid repression by EZH2 and FOXO1 in prostate cancer and Ewing sarcoma." Cancer Research 84, no. 6_Supplement (2024): 3033. http://dx.doi.org/10.1158/1538-7445.am2024-3033.

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Abstract ETS transcription factors play roles throughout development, aiding in hematopoiesis, blood vessel formation and cell fate. The ETS family is composed of 28 members, all of which share an ETS DNA-binding domain. Chromosomal rearrangements that lead to the overexpression of specific ETS promote oncogenic transformation and tumor development. More than half of prostate tumors are driven by aberrant expression of an ETS protein. Our lab has demonstrated that oncogenic ETS form essential interactions with a ubiquitous RNA-binding protein, EWS, to promote prostate tumorigenesis. A similar

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11

Clark, Jeremy P., and Colin S. Cooper. "ETS gene fusions in prostate cancer." Nature Reviews Urology 6, no. 8 (2009): 429–39. http://dx.doi.org/10.1038/nrurol.2009.127.

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12

Gleave, Martin, Eric Belanger, Joshua Scurll, et al. "Genomic alterations and their pathologic responses in high-risk localized prostate cancer (HRLPC) in subprotocol 1 of the Genomic Umbrella Neoadjuvant study (GUNS)." Journal of Clinical Oncology 43, no. 5_suppl (2025): 403. https://doi.org/10.1200/jco.2025.43.5_suppl.403.

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403 Background: GUNS (NCT04812366) is a multicenter adaptive phase II trial evaluating 24 weeks of biomarker-selected, neoadjuvant androgen receptor pathway inhibitor (ARPI) combination therapies on depth of pathologic response (complete response [pCR] or <5 mm minimal residual disease [MRD]) in HRLPC. After 8 weeks of LHRHa + apalutamide (APA), participants are assigned to 1 of 4 sub-protocols (SP) combining 16 weeks of an ARPI doublet with drugs defined by specific genomic alterations (e.g. SP-2, docetaxel for RB1 , PTEN , TP53 loss; SP-3, niraparib for DNA-repair def ; SP-4, atezolizumab

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13

Deneen, Benjamin, Scott M. Welford, Thu Ho, Felicia Hernandez, Irwin Kurland, and Christopher T. Denny. "PIM3 Proto-Oncogene Kinase Is a Common Transcriptional Target of Divergent EWS/ETS Oncoproteins." Molecular and Cellular Biology 23, no. 11 (2003): 3897–908. http://dx.doi.org/10.1128/mcb.23.11.3897-3908.2003.

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ABSTRACT Despite significant structural diversity, present evidence suggests that EWS/ETS fusion proteins promote oncogenesis by transcriptionally modulating a common set of target genes. In order to identify these genes, microarray expression analyses were performed on NIH 3T3 polyclonal populations expressing one of three EWS/ETS fusion genes. The majority of these genes can be grouped into seven functional categories, including cellular metabolism and signal transduction. The biologic significance of these target genes was pursued. The effects of modulating genes involved in metabolism were

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14

Mani, Ram-Shankar, Scott A. Tomlins, Kaitlin Callahan, et al. "Induced Chromosomal Proximity and Gene Fusions in Prostate Cancer." Science 326, no. 5957 (2009): 1230. http://dx.doi.org/10.1126/science.1178124.

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Gene fusions play a critical role in cancer progression. The mechanisms underlying their genesis and cell type specificity are not well understood. About 50% of human prostate cancers display a gene fusion involving the 5′ untranslated region of TMPRSS2, an androgen-regulated gene, and the protein-coding sequences of ERG, which encodes an erythroblast transformation–specific (ETS) transcription factor. By studying human prostate cancer cells with fluorescence in situ hybridization, we show that androgen signaling induces proximity of the TMPRSS2 and ERG genomic loci, both located on chromosome

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15

Hussain, Maha, Stephanie Daignault-Newton, Przemyslaw W. Twardowski, et al. "Targeting Androgen Receptor and DNA Repair in Metastatic Castration-Resistant Prostate Cancer: Results From NCI 9012." Journal of Clinical Oncology 36, no. 10 (2018): 991–99. http://dx.doi.org/10.1200/jco.2017.75.7310.

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Purpose To determine whether cotargeting poly (ADP-ribose) polymerase-1 plus androgen receptor is superior to androgen receptor inhibition in metastatic castration-resistant prostate cancer (mCRPC) and whether ETS fusions predict response. Patients and Methods Patients underwent metastatic site biopsy and were stratified by ETS status and randomly assigned to abiraterone plus prednisone without (arm A) or with veliparib (arm B). Primary objectives were: confirmed prostate-specific antigen (PSA) response rate (RR) and whether ETS fusions predicted response. Secondary objectives were: safety, me

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16

Zou, Ying S., Laura Morsberger, Melanie Hardy, et al. "Complex/cryptic EWSR1::FLI1/ERG Gene Fusions and 1q Jumping Translocation in Pediatric Ewing Sarcomas." Genes 14, no. 6 (2023): 1139. http://dx.doi.org/10.3390/genes14061139.

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Ewing sarcomas (ES) are rare small round cell sarcomas often affecting children and characterized by gene fusions involving one member of the FET family of genes (usually EWSR1) and a member of the ETS family of transcription factors (usually FLI1 or ERG). The detection of EWSR1 rearrangements has important diagnostic value. Here, we conducted a retrospective review of 218 consecutive pediatric ES at diagnosis and found eight patients having data from chromosome analysis, FISH/microarray, and gene-fusion assay. Three of these eight ES had novel complex/cryptic EWSR1 rearrangements/fusions by c

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17

Zhang, Yue. "Article Commentary: ETS-FUSions Networking, Triggering and Beyond." Genetics & Epigenetics 3 (January 2010): GEG.S4166. http://dx.doi.org/10.4137/geg.s4166.

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Gene fusion is a hallmark of cancer development with the mechanisms underlying their genesis emerging. The Staege and Max paper together with another recent paper have provided a comprehensive first view on current TET-ETS translocation studies. This significance, the trigering of gene fusion and beyond will be discussed in this article.

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18

Feng, Felix Y., J. Chad Brenner, Maha Hussain, and Arul M. Chinnaiyan. "Molecular Pathways: Targeting ETS Gene Fusions in Cancer." Clinical Cancer Research 20, no. 17 (2014): 4442–48. http://dx.doi.org/10.1158/1078-0432.ccr-13-0275.

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19

Yoshimoto, M., A. M. Joshua, S. Chilton-Macneill, et al. "Detection of novel variant TMPRSS2 /ERG fusion transcripts suggests independent genomic alterations may underlie origin of multi-centric prostate cancer." Journal of Clinical Oncology 24, no. 18_suppl (2006): 10029. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10029.

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10029 Background: Most of the early successes in identifying chromosomal translocations in neoplasias came from the study of hematological malignancies and sarcomas, with limited evidence that consistent genomic rearrangements were present in epithelial malignancies. Recently it was reported that ∼75% of prostate cancers carry a genomic rearrangement leading to fusion of the TMPRSS2 locus to either the ERG or ETV1 genes (both ETS transcription factors). In the fusion gene, the androgen-sensitive promoter elements of TMPRSS2 are thought to mediate over-expression of these ETS transcription fact

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20

He, Wei, Fukang Sun, Juping Zhao, et al. "Prevalence and genetic features of TMPRSS2-ERG fusion in Chinese patients with prostate cancer." Journal of Clinical Oncology 38, no. 15_suppl (2020): e17529-e17529. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e17529.

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e17529 Background: Prostate cancer (PCa) is one of the most common malignancies, with rising incidence rate in China. The Cancer Genome Atlas (TCGA) revealed 53% of patients with PCa had ETS family gene fusions. The most frequent fusion type of ETS fusions is TMPRSS2-ERG, which may predicts resistance to taxane and androgen-deprivation therapies. The prevalence of TMPRSS2-ERG fusion in Chinese PCa patients evaluated by fluorescence in situ hybridization (FISH) or immunohistochemistry (IHC) varied from 7.5% to 78.0%. However, the sample sizes were small. In the present study, we investigated th

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21

Arvand, Afsane, and Christopher T. Denny. "Biology of EWS/ETS fusions in Ewing's family tumors." Oncogene 20, no. 40 (2001): 5747–54. http://dx.doi.org/10.1038/sj.onc.1204598.

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22

Khosh Kish, Ealia, Muhammad Choudhry, Yaser Gamallat, Sabrina Marsha Buharideen, Dhananjaya D, and Tarek A. Bismar. "The Expression of Proto-Oncogene ETS-Related Gene (ERG) Plays a Central Role in the Oncogenic Mechanism Involved in the Development and Progression of Prostate Cancer." International Journal of Molecular Sciences 23, no. 9 (2022): 4772. http://dx.doi.org/10.3390/ijms23094772.

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The ETS-related gene (ERG) is proto-oncogene that is classified as a member of the ETS transcription factor family, which has been found to be consistently overexpressed in about half of the patients with clinically significant prostate cancer (PCa). The overexpression of ERG can mostly be attributed to the fusion of the ERG and transmembrane serine protease 2 (TMPRSS2) genes, and this fusion is estimated to represent about 85% of all gene fusions observed in prostate cancer. Clinically, individuals with ERG gene fusion are mostly documented to have advanced tumor stages, increased mortality,

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23

Khosh Kish, Ealia, Muhammad Choudhry, Yaser Gamallat, Sabrina Marsha Buharideen, Dhananjaya D, and Tarek A. Bismar. "The Expression of Proto-Oncogene ETS-Related Gene (ERG) Plays a Central Role in the Oncogenic Mechanism Involved in the Development and Progression of Prostate Cancer." International Journal of Molecular Sciences 23, no. 9 (2022): 4772. http://dx.doi.org/10.3390/ijms23094772.

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The ETS-related gene (ERG) is proto-oncogene that is classified as a member of the ETS transcription factor family, which has been found to be consistently overexpressed in about half of the patients with clinically significant prostate cancer (PCa). The overexpression of ERG can mostly be attributed to the fusion of the ERG and transmembrane serine protease 2 (TMPRSS2) genes, and this fusion is estimated to represent about 85% of all gene fusions observed in prostate cancer. Clinically, individuals with ERG gene fusion are mostly documented to have advanced tumor stages, increased mortality,

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24

Zhang, Zhusheng, Qiyuan Bao, Junxiang Wen, et al. "Abstract 4545: Integrative immune-genomic comparison of canonical Ewing sarcoma with Ewing-like mimics identifies potential targets for personalized therapies." Cancer Research 83, no. 7_Supplement (2023): 4545. http://dx.doi.org/10.1158/1538-7445.am2023-4545.

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Abstract Introduction: Ewing sarcoma (ES) is one of the most common types of small round cell sarcoma (SRCS) from the skeletal origin, characterized by small round blue cell morphology and FET-ETS fusions. However, recent NGS-based technology has dramatically increased the characterization of other SRCS entities that share morphological, pathological, and clinical similarity with canonical ES. Currently, these sarcomas are often treated with similar regimens derived from ES. Whether any subsets of these sarcomas might benefit from personalized anti-cancer strategies remains largely unknown. Me

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Le Deley, Marie-Cecile, Olivier Delattre, Karl-Ludwig Schaefer, et al. "Impact of EWS-ETS Fusion Type on Disease Progression in Ewing's Sarcoma/Peripheral Primitive Neuroectodermal Tumor: Prospective Results From the Cooperative Euro-E.W.I.N.G. 99 Trial." Journal of Clinical Oncology 28, no. 12 (2010): 1982–88. http://dx.doi.org/10.1200/jco.2009.23.3585.

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Purpose EWS-ETS fusion genes are the driving force in Ewing's sarcoma pathogenesis. Because of the variable breakpoint locations in the involved genes, there is heterogeneity in fusion RNA and protein architecture. Since previous retrospective studies suggested prognostic differences among patients expressing different EWS-FLI1 fusion types, the impact of fusion RNA architecture on disease progression and relapse was studied prospectively within the Euro-E.W.I.N.G. 99 clinical trial. Patients and Methods Among 1,957 patients who registered before January 1, 2007, 703 primary tumors were access

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Anderson, Peter Meade, Luisa-Marie Manning, Brian Rubin, et al. "Nested set information derived from fusion genes in Ewing sarcoma and other cancers." Journal of Clinical Oncology 40, no. 16_suppl (2022): e23521-e23521. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e23521.

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e23521 Background: Ewing family tumors including Ewing sarcoma (ES) and desmoplastic small round cell tumor (DSRCT) are characterized by EWSR1 and ETS fusion partners including EWS-FLI1, EWS-ERG, EWS-WT1, and others. Since 2019 our Next Generation Sequencing (NGS) sarcoma panel (N = 338) identified both fusion partners and exons containing the EWS breakpoint in ES and DSRCT. Hence, it should be possible to learn more about the exact breakpoints of EWS fusion genes. The molecular diversity and functionality of these fusion transcripts, especially the exact sequence, which could be identical, si

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27

Feng, Felix Yi-Chung, Scott Tomlins, Mohammed Alshalalfa, et al. "Molecular and clinical characterization of 1,577 primary prostate cancer tumors to reveal novel clinical and biological insights into its subtypes." Journal of Clinical Oncology 33, no. 7_suppl (2015): 9. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.9.

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9 Background: Prostate cancer molecular subtypes based on ETS gene fusions and SPINK1 were originally identified through outlier gene expression profiling analysis. Such molecular subtypes may have utility in disease stratification and clonality assessment, complementing available purely prognostic tests. Hence, we determined the analytical validity of molecular subtyping in a large sample of PCa treated with radical prostatectomy. Methods: We analyzed Affymetrix Human Exon 1.0ST GeneChip expression profiles for 1,577 patients from 8 radical prostatectomy (RP) cohorts. Multi-feature random for

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Downing, Nicholas Frederick, Katelyn M. Mills, and Peter C. Hollenhorst. "Abstract 4038: Oncogenic ETS transcription factors in prostate cancer and Ewing sarcoma are interchangeable when avoiding repression by a PRC2/FOXO1 complex." Cancer Research 85, no. 8_Supplement_1 (2025): 4038. https://doi.org/10.1158/1538-7445.am2025-4038.

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Abstract ETS transcription factors play roles throughout development, aiding in hematopoiesis, blood vessel formation and cell fate. The ETS family is composed of 28 members, all of which share an ETS DNA-binding domain. Chromosomal rearrangements that lead to the overexpression of specific ETS promote oncogenic transformation and tumor development. More than half of prostate tumors are driven by aberrant expression of an ETS protein. Our lab has demonstrated that oncogenic ETS form essential interactions with a ubiquitous RNA-binding protein, EWS, to promote prostate tumorigenesis. A similar

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29

Smit, F. P., M. Salagierski, D. Hessels, S. A. Jannink, and J. A. Schalken. "786 IDENTIFICATION OF ETS GENE FUSIONS USING AFFYMETRIX EXON 1.0 ARRAYS." European Urology Supplements 8, no. 4 (2009): 317. http://dx.doi.org/10.1016/s1569-9056(09)60774-0.

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30

Hammer, Liat, Ryan Rebernick, Matthew McFarlane, et al. "Clinical impact of mutations in driver oncogenes and TP53/RB1 in advanced prostate cancer." Journal of Clinical Oncology 41, no. 6_suppl (2023): 263. http://dx.doi.org/10.1200/jco.2023.41.6_suppl.263.

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263 Background: Prostate cancer (PCa) is characterized by considerable genetic heterogeneity, and complex genomic features may influence prognosis and treatment response. We created a database of aggressive PCa that integrates comprehensive genomic sequencing with detailed clinical outcomes to better understand the optimal use of genomic sequencing. Methods: From 4/2005-7/2021, PCa cancer patients older than 18 years of age underwent tissue collection for tumoral RNA-sequencing and tumor/normal whole exome sequencing at our institution (HUM00046018, HUM00048105, HUM00067928, SU2C). Genomic and

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Yaseen, Nabeel R., Akiko Takeda, Reza Nazari, Helen Shio, Gunter Blobel, and Hualin Zhong. "Carrier-Independent Nuclear Import of the Transcription Factor PU.1." Blood 104, no. 11 (2004): 3561. http://dx.doi.org/10.1182/blood.v104.11.3561.3561.

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Abstract PU.1 is a transcription factor of the Ets family with important functions in hematopoietic cell differentiation. Using GFP-PU.1 fusions, we show that the Ets DNA-binding domain of PU.1 is necessary and sufficient for its nuclear localization. Fluorescence and ultrastructural nuclear import assays showed that PU.1 nuclear import requires energy but not soluble carriers. PU.1 interacted with the FG repeats of nucleoporins Nup62 and Nup153. The binding of PU.1 to Nup153, but not to Nup62, dramatically increased in the presence of RanGMPPNP, indicating the formation of a PU.1/RanGTP/Nup15

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32

Ho, Jen M. Y., Bryan K. Beattie, Jeremy A. Squire, David A. Frank, and Dwayne L. Barber. "Fusion of the ets Transcription Factor TEL to Jak2 Results in Constitutive Jak-Stat Signaling." Blood 93, no. 12 (1999): 4354–64. http://dx.doi.org/10.1182/blood.v93.12.4354.

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Abstract To study constitutive Janus kinase signaling, chimeric proteins were generated between the pointed domain of the etstranscription factor TEL and the cytosolic tyrosine kinase Jak2. The effects of these proteins on interleukin-3 (IL-3)–dependent proliferation of the hematopoietic cell line, Ba/F3, were studied. Fusion of TEL to the functional kinase (JH1) domain of Jak2 resulted in conversion of Ba/F3 cells to factor-independence. Importantly, fusion of TEL to the Jak2 pseudokinase (JH2) domain or a kinase-inactive Jak2 JH1 domain had no effect on IL-3–dependent proliferation of Ba/F3

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Ho, Jen M. Y., Bryan K. Beattie, Jeremy A. Squire, David A. Frank, and Dwayne L. Barber. "Fusion of the ets Transcription Factor TEL to Jak2 Results in Constitutive Jak-Stat Signaling." Blood 93, no. 12 (1999): 4354–64. http://dx.doi.org/10.1182/blood.v93.12.4354.412k30_4354_4364.

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To study constitutive Janus kinase signaling, chimeric proteins were generated between the pointed domain of the etstranscription factor TEL and the cytosolic tyrosine kinase Jak2. The effects of these proteins on interleukin-3 (IL-3)–dependent proliferation of the hematopoietic cell line, Ba/F3, were studied. Fusion of TEL to the functional kinase (JH1) domain of Jak2 resulted in conversion of Ba/F3 cells to factor-independence. Importantly, fusion of TEL to the Jak2 pseudokinase (JH2) domain or a kinase-inactive Jak2 JH1 domain had no effect on IL-3–dependent proliferation of Ba/F3 cells. Ac

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34

Feng, F. Y., S. Han, C. Brenner, et al. "PARP inhibition reverses radiation resistance conferred by ETS fusions in prostate cancer." Journal of Clinical Oncology 29, no. 15_suppl (2011): 4545. http://dx.doi.org/10.1200/jco.2011.29.15_suppl.4545.

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35

Tomlins, Scott A., Anders Bjartell, Arul M. Chinnaiyan, et al. "ETS Gene Fusions in Prostate Cancer: From Discovery to Daily Clinical Practice." European Urology 56, no. 2 (2009): 275–86. http://dx.doi.org/10.1016/j.eururo.2009.04.036.

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36

Dong, Rongfang, Lan Li, Lihua Gong, et al. "Abstract 2152: Targetable oncogenic fusions and other alterations in bone and soft-tissue tumors assessed by RNA and DNA-based next-generation sequencing in real-world experience." Cancer Research 83, no. 7_Supplement (2023): 2152. http://dx.doi.org/10.1158/1538-7445.am2023-2152.

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Abstract Background: Bone and soft-tissue tumors, especially soft-tissue sarcoma may have an underlying genetic mechanism, where fusion oncoproteins serve as drivers of the disease. This genetic simplicity provides an exceptional opportunity to develop effective and specific therapies. Here, we used RNA and DNA- based next-generation sequencing (NGS) to identify potentially druggable oncogene fusions in our patients that can be used for clinical trial involvement. Methods: Pediatric and adult patients with bone and soft tissue tumors treated in our hospital undergoing biopsy or surgery were en

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Bilke, Sven, Raphaela Schwentner, Fan Yang, et al. "Oncogenic ETS fusions deregulate E2F3 target genes in Ewing sarcoma and prostate cancer." Genome Research 23, no. 11 (2013): 1797–809. http://dx.doi.org/10.1101/gr.151340.112.

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Tomlins, Scott A., Bharathi Laxman, Saravana M. Dhanasekaran, et al. "Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer." Nature 448, no. 7153 (2007): 595–99. http://dx.doi.org/10.1038/nature06024.

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Dehm, Scott M. "Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer." Urologic Oncology: Seminars and Original Investigations 26, no. 6 (2008): 687–88. http://dx.doi.org/10.1016/j.urolonc.2008.09.003.

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Dong, Jun, Li Xiao, Lu Sheng, Jun Xu, and Zhong-Quan Sun. "TMPRSS2:ETS Fusions and Clinicopathologic Characteristics of Prostate Cancer Patients from Eastern China." Asian Pacific Journal of Cancer Prevention 15, no. 7 (2014): 3099–103. http://dx.doi.org/10.7314/apjcp.2014.15.7.3099.

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Dan, Yuqing, Ruibao Ren, Donghe Li, and Ping Liu. "Novel Fusion Gene Aven-NUTM1 Induces Mice Myeloid Leukemia Vulnerable to HDAC Inhibitors." Blood 142, Supplement 1 (2023): 4123. http://dx.doi.org/10.1182/blood-2023-188034.

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Chromosomal rearrangements involving the NUTM1 gene produce fusion genes commonly found in NUT carcinoma. While recurring NUTM1 fusions have been reported in other neoplasms, including AML, their roles in leukemogenesis remain unclear. We identified the AVEN-NUTM1 (AN) fusion gene in an AML patient resistant to standard chemotherapy, and went to assess AN's leukemogenicity via bone marrow transduction and transplantation. Mice transplanted with AN-transduced hematopoietic stem/progenitor cells (HSPCs) developed transplantable myeloid leukemia with a median survival of 342 days. RNA sequencing

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Cools, Jan, Chrystèle Bilhou-Nabera, Iwona Wlodarska, et al. "Fusion of a Novel Gene, BTL, to ETV6 in Acute Myeloid Leukemias With a t(4;12)(q11-q12;p13)." Blood 94, no. 5 (1999): 1820–24. http://dx.doi.org/10.1182/blood.v94.5.1820.

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Abstract The ETV6 gene (also known as TEL) is the main target of chromosomal translocations affecting chromosome band 12p13. The rearrangements fuse ETV6 to a wide variety of partner genes in both myeloid and lymphoid malignancies. We report here 4 new cases of acute myeloid leukemia (AML) with very immature myeloblasts (French-American-British [FAB]-M0) and with a t(4;12)(q11-q12;p13). In all cases, ETV6 was found recombined to a new gene, homologous to the mouse Brx gene. The gene was named BTL (Brx-likeTranslocated in Leukemia). Reverse transcriptase-polymerase chain reaction (RT-PCR) exper

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Cools, Jan, Chrystèle Bilhou-Nabera, Iwona Wlodarska, et al. "Fusion of a Novel Gene, BTL, to ETV6 in Acute Myeloid Leukemias With a t(4;12)(q11-q12;p13)." Blood 94, no. 5 (1999): 1820–24. http://dx.doi.org/10.1182/blood.v94.5.1820.417k09_1820_1824.

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The ETV6 gene (also known as TEL) is the main target of chromosomal translocations affecting chromosome band 12p13. The rearrangements fuse ETV6 to a wide variety of partner genes in both myeloid and lymphoid malignancies. We report here 4 new cases of acute myeloid leukemia (AML) with very immature myeloblasts (French-American-British [FAB]-M0) and with a t(4;12)(q11-q12;p13). In all cases, ETV6 was found recombined to a new gene, homologous to the mouse Brx gene. The gene was named BTL (Brx-likeTranslocated in Leukemia). Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments in

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Hong, J., J. Markidan, T. Helm, K. Helm, and T. Thieu. "ALK1-negative Epithelioid Histiocytoma." American Journal of Clinical Pathology 162, Supplement_1 (2024): S30—S31. http://dx.doi.org/10.1093/ajcp/aqae129.066.

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Abstract Introduction/Objective We present a case of epithelioid histiocytoma (EH). The epithelioid nature of this lesion imitates the appearance of neoplastic lesions such as melanocytic, dermatofibroma/histiocytoma, non-Langerhans histiocytosis such as reticulohistiocytoma, atypical fibroxanthoma, and rhabdomyosarcoma. Methods/Case Report Due to the unusual morphology and aberrant immunohistochemical staining pattern of this specific case, the sample was analyzed through Next Generation Sequencing (NGS), which showed the presence of a fusion of genes Sequestosome 1 (SQSTM1) and Anaplastic ly

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Seligson, Nathan David, Richard D. Maradiaga, Colin W. Stets, et al. "Multiscale omic assessment of EWSR1-NFATc2 fusion positive sarcomas to identify conserved fusion breakpoint and activation of the mTOR pathway." Journal of Clinical Oncology 38, no. 15_suppl (2020): e23536-e23536. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e23536.

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e23536 Background: EWSR1-NFATc2 ( E-N) fusion positive sarcomas are rare cancers historically categorized as Ewing sarcomas. Emerging evidence suggests unique molecular characteristics and chemotherapy sensitivities in these cancers. Here we present the largest cohort of genomically profiled E-N fusion positive sarcomas and evaluate their breakpoints and putative pathway alterations. Methods: Comprehensive genomic profiling of 1,024 EWSR1 fusion positive sarcomas, including 14 E-N fusions, was obtained through the Foundation Medicine research database (FMI). Additional data from the Gene Expre

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Thompson, Andrew D., Michael A. Teitell, Afsane Arvand, and Christopher T. Denny. "Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells." Oncogene 18, no. 40 (1999): 5506–13. http://dx.doi.org/10.1038/sj.onc.1202928.

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Braunreiter, Chi L., Jeffery D. Hancock, Cheryl Coffin, Kenneth M. Boucher, and Stephen L. Lessnick. "Expression of EWS-ETS Fusions in NIH3T3 Cells Reveals Significant Differences to Ewing’s Sarcoma." Cell Cycle 5, no. 23 (2006): 2753–59. http://dx.doi.org/10.4161/cc.5.23.3505.

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Paulo, Paula, João D. Barros-Silva, Franclim R. Ribeiro, et al. "FLI1 is a novel ETS transcription factor involved in gene fusions in prostate cancer." Genes, Chromosomes and Cancer 51, no. 3 (2011): 240–49. http://dx.doi.org/10.1002/gcc.20948.

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GUO, Xiao-Qiang, Yao-Ting GUI, and Zhi-Ming CAI. "The progress of TMPRSS2-ETS gene fusions and their mechanism in prostate cancer." Hereditas (Beijing) 33, no. 2 (2011): 117–22. http://dx.doi.org/10.3724/sp.j.1005.2011.00117.

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Pflueger, D., S. Terry, A. Sboner, et al. "Discovery of non-ETS gene fusions in human prostate cancer using next-generation RNA sequencing." Genome Research 21, no. 1 (2010): 56–67. http://dx.doi.org/10.1101/gr.110684.110.

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